Capsular contracture around breast prostheses is the principal cause for dissatisfaction in breast augmentation. All breast prosthesis are soft, pliable and adjust to a pleasing shape when first installed; but the body's response to the presence of the implant may later cause contracture. Alterations must be made in the prosthesis or the body's response to affect the capsule formation in the future. McGrath and Burkhardt, "The Safety and Efficacy of Breast Implants for Augmentation Mammoplasty", Plastic Reconstr. Surg., 74:550-560 (1984), have published an extensive review of certain developments and also difficulties in attempting to control scar tissue formation around soft silicone implants. In some 251 studies, it was shown that up to 74% develop contractures, but only one-half are bilateral. The disease is capsular contracture (the problem being believed to be created by the contractile myofibroblast) and the mechanism has been studied and described. The contributing factors of infection, inflammation, hematoma formation and unknown factors all lead to increased scar formation. Attempts to alter this basic response have been diverse and evolving over many years. These studies were designed to alter the surface morphology of the prosthesis so as to influence the capsule's characteristics for softer breasts.
One of the most fertile frontiers of plastic surgery is the host prosthesis interface. The development of dependable prosthetic devices is generally directed or related to the creation of a non-space between the host and the prosthesis. The earliest advances in prosthetic implantation were made when a variety of substances were discovered and developed that were relatively inert so they could remain in tissue without disturbing the physiology of the host. All implants elicit a foreign body reaction, and all implants are subject to an initial inflammatory phase where the host attempts to either eliminate or encapsulate the prosthesis. Control of this inflammation and encapsulation may be achieved by altering the host-prosthesis interface. The inflammatory phase of wound healing lasts for about one week; the phase of fibrosis or collagen deposition begins and increases for a few weeks. Once encapsulation is complete, collagen deposition and degradation approach equilibrium and the scar matures within 30-60 days if the host is in good health and no outside forces influence the host-prosthesis interface. In the case of structurally hard substances such as ceramics, stainless steel, and other inert metals and hard plastics, the amount and degree of encapsulation does not affect their function, but only their fixation. The stability of bone prostheses is greatly enhanced if tissue, particularly bone tissue ingrowth can be induced. This has been accomplished in the past by sintering or texturing the surface or attaching porous substance that would allow some tissue ingrowth. Where silicone rubber blocks and pre-formed prosthetics, which in the nose, and other sites, were function-dependent on form, encapsulation proceeded in a similar way and was not a problem. Fibroblasts actually migrate along a substrata (plastic) and lay down collagen as a mirror image of the substrate through contact guidance. Fibrosis and increased collagen production cease when fibroblasts contact other fibroblasts, normally termed contact inhibition.
The development, however, of soft, pliable prosthetic implants for breast enlargement and other body contour problems has been successful to the extent that the foreign body reaction could be minimized, and initially, the host prosthesis interface was made as smooth as possible. It was hoped that this smooth surface would elicit a minimal foreign body reaction, and since silicone rubber is a relatively inert substance, it would be ignored by the body. Indeed, this was found to be true in most cases. This smooth surface, however, prevents any attachment of the scar capsule to the prosthesis so that any movement of the host creates a shearing effect if any microscopic surface irregularity, such as the edge of a fill patch or a mold seam or a fold flaw corner. However, if inflammation was increased by local infection or inadvertent hematoma formed, the amount of fibrosis was greatly increased. If after a long quiescent period of pliability and stability, the prosthesis was subject to trauma, so that subcapsular bleeding ensued, or infection in a nearby area unrelated to the surgery caused increased inflammation and scar tissue, an encapsulation response was often elicited even though many months or years of soft quiescent implantation had preceded.
As early as 1969 successes were achieved in altering the surface characteristics of tetrafluoroethylene (Teflon-trademark of the du Pont Company of Wilmington, Del.) implants by texturing, this allowing for an intimate, flexible host-prosthesis interface to be developed with a thinner encapsulation with random axis collagen fibrils and a firm mechanical bond between the inert tetrafluoroethylene (Teflon) and the host, including both animals and humans. In these experiments and clinical applications, a waterproof, germ-proof seal was created between the host and inert tetrafluoroethylene (Teflon) prosthesis that was a thin stable scar, when compared to the chronic inflammatory, thick scar pseudo-bursa around the smooth shunts. Other controlled studies have shown inert textured tetrafluoroethylene (Teflon) in rabbits creates a thinner capsule.
In subsequent work with semi-synthetic implants, such as human umbilical cords and vascular conduits, it was found that the outer surface, being textured by a mechanical process to create a net-like textured surface, allowed for the intimate intertwining of the capsule collagen and the interstices of the texturing, so that an effective host prosthesis interface would be developed that would prevent perigraft pseudoaneurysms, even in the face of repeated punctures, as in dialysis access. The previous work with the semi-synthetic glutaraldehyde cross-linked chondroplast in monkeys showed that the classic foreign body reaction and encapsulation resulted in a scalloping or texturing of the surface of this otherwise smooth substance. This texturing was shown to create an effective host prosthesis interface with a minimal encapsulation response and a thinner capsule with multi-planar random axis orientation of the fibers. When compared with silicone rubber blocks in the same animal, in the same site, at the same time, it was noted that the textured chondroplast elicited a thinner capsule and on electron-microscopy, this thin capsule had a cellular surface with few free collagen fibrils. The seemingly smooth silicone rubber, however, elicited a four times thicker mono-planar aligned capsule with a surface of free fibrils of collagen.
Taylor and Gibbons ("Effective Surface Texture on the Soft Tissue Response to Polymer Implants", Journal of Biomedical Materials Research, 17:205-277 (1984)), have shown that just altering the surface texture of inert tetrafluoroethylene (Teflon) alters the host response as a result of that texture. Specifically, this texturing of tetrafluoroethylene (Teflon) in their studies resulted in a thinner capsule with less cellular activity than a perfectly smooth implant of the same material in the same animal at the same time. Their work implies that texturing prevents the host prosthesis interface action (micromotion) with its repeated mechanical trauma to the surface cell. Texturing the surface of a prosthesis to prevent chest wall adhesion to the myocardium and following cardiac surgery has shown that the textured surface aids the host in isolating and destroying infection, whereas smooth, seemingly serosal surfaces allow for the rapid spread of infection.
These earlier experiments and observations have led to the improvements of the present invention, including development of surface textured implants to allow for the mechanical ingrowth of host fibrous tissue to produce a mechanical bond of the host prosthesis interface and prevent micromotion. It appears that the texturing of the surface in accordance with the present invention allows for the fibroblast to grow into and around the interstices of the surface and thus, at least on several planes, touch another fibroblast. The capsule of the textured surface has collagen fibers that are arranged in a random axis pattern that generally follows the random directions of the textured surface, and this way, the contractile forces of the contractile myofibroblasts to some extent cancel each other out. Recent papers of others support this concept.
The human fibroblast is described as a pleomorphic cell of mesenchymal origin. This cell is approximately 20 to 100 microns in size. Therefore, in order to have any effect on the configuration of the capsule produced by these fibroblasts, it has been determined that indentations must be at least in the 20 to 100 micron range. Texturing with hills and valleys greater than 2 mm. might alter the surface so drastically as to be seen or felt through the skin of a thin-skinned individual. By impacting the surface of silicone implants prior to vulcanization, it is possible to create surfaces that approximate the desired irregularities as hills and valleys in a net-like three-dimensional grid. It is possible to create a reverse image of an imaginary fibroblast colony by creating "designer molecules" to create a friendly environment for the host cells. This method provides a variety of precise hills and valleys wherein few of the indentations communicate with each other, but the hills have very irregular surfaces. The use of open-cell foam may allow some tissue ingrowth on the surface, but it also produces unfathomable caves and indentations where bacteria may thrive. Contact inhibition by these random axis fibroblasts may result in a thinner capsule formation. The textured accordion-pleat like surfaces may allow for some spring-like expansion of the surface. This is generally the random direction of collagen found in skin, which is flexible. The smooth surfaced prosthesis, however, elicits a fibrous reaction wherein all of the collagen fibrils are aligned, in a cumulative manner, in one spherical plane. This way, the contractile forces of the contractile myofibroblasts, if stimulated, will be parallel and tangential to the surface of the prosthesis, since it is a continuous surface. This is the exact configuration of collagen in tendons, which does not yield. All of these additive forces are in parallel alignment.
Attempts by others to use polyurethane foam and polyethylene terephthalate (Dacron-trademark of the du Pont Company of Wilmington, Del.) fabric and other substances has led to some earlier reports of improved host prosthesis interface reaction because of these mechanical factors. However, since the polyurethane foam biodegrades into questionable substances and since the disappearance of the urethane leaves a partially smooth silicone prosthesis after some period of time, its benefits appear to be temporary at best. In addition, the late infection rate of this urethane foam may be related to the chronic inflammatory response that may cause a pink rash and softer prosthesis. By texturing silicone rubber in a predetermined pattern, we may be able to alter the host response to wound healing now, so that tissue ingrowth may produce the host prosthesis interface that would be more stable, more compatible, thinner and remain soft longer, and decrease capsular contracture in the future.